Serum Lp(a) Levels in Patients with Moderate Renal Failure

Bairaktari, Eleni; Elisaf, Moses; Tsolas, O.; Siamopoulos, Kostas C.

doi:10.1159/000045073

Cited by 17 publications

(9 citation statements)

References 8 publications

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“…The inverse correlation between serum Lp(a) and creatinine in cross-sectional studies examining patients with mild to moderate renal failure and a frequency of distribution of apo(a) isoforms similar to controls suggest that the renal insufficiency itself is responsible for the increased Lp(a) levels [21,22,23]. Our data are consistent with other prospective studies that have shown decreases of Lp(a) after transplantation several months to years post-transplant [24,25,26,27].…”

Section: Discussionmentioning

confidence: 99%

Effects of Renal Replacement Therapy on Plasma Lipoprotein(a) Levels

Rosas¹,

Joffe

Wolfe

et al. 2007

Am J Nephrol

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Patients with end-stage renal disease (ESRD) have significantly higher levels of lipoprotein(a) [Lp(a)] when compared to control populations. Elevated levels of Lp(a) may play a role in the high incidence of cardiovascular disease in ESRD. We conducted a prospective study to test the hypothesis that plasma levels of Lp(a) decline rapidly after renal transplantation proportional to the improvement in renal function, but are not affected by hemodialysis. All adults that initiated hemodialysis or received a renal transplant from our institution during a 10-month period were invited to participate in the study. Lp(a) levels were obtained immediately prior to the initiation of renal replacement therapy. In transplant recipients, repeat Lp(a) measures were done at 3 days, 5 days, 1 week, 2 weeks, 3 weeks and 4 weeks post-transplant. In hemodialysis patients, repeat Lp(a) measures were done after 3 months. We used a mixed effects model to analyze the effect of time, race and creatinine on Lp(a) after transplant. Lp(a) levels decreased rapidly after renal transplantation. Mean Lp(a) levels at 2 weeks were 35.3% lower than prior to transplantation. Each reduction of 50% in creatinine was associated with a 10.6% reduction in Lp(a) (p < 0.001). In contrast, there was no significant change in Lp(a) after initiation of hemodialysis. The rapid decrease of Lp(a) levels after renal transplantation provides support for a metabolic role of the kidney in Lp(a) catabolism and suggests that the increase in Lp(a) seen in chronic kidney disease is due to loss of functioning renal tissue.

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Section: Discussionmentioning

confidence: 99%

Effects of Renal Replacement Therapy on Plasma Lipoprotein(a) Levels

Rosas¹,

Joffe

Wolfe

et al. 2007

Am J Nephrol

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“…The large concentration gradient of Lp(a) between aorta and the renal vein [71] as well as the identification of apo(a) fragments in urine [72] suggest that the kidney may actively participate in the degradation of Lp(a). Thus, it is not surprising that patients with primary kidney diseases (even those with normal GFR values) usually exhibit markedly elevated concentrations of Lp(a) [73, 74] as well as increased concentrations of LDL-unbound apo(a) [75]. However, recently published studies indicate that the negative association between renal function and Lp(a) levels is phenotype-specific.…”

Section: Lipoprotein (A) (Lp(a)) and Ckdmentioning

confidence: 99%

Dyslipidemia Associated with Chronic Kidney Disease

Tsimihodimos

Mitrogianni²,

Elisaf

2011

TOCMJ

141

129

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Cardiovascular disease is a major cause of morbidity and mortality in patients with impaired renal function. Dyslipidemia has been established as a well-known traditional risk factor for cardiovascular disease (CVD) in the general population and it is well known that patients with chronic kidney disease (CKD) exhibit significant alterations in lipoprotein metabolism. In this review, the pathogenesis and treatment of CKD-induced dyslipidemia are discussed. Studies on lipid abnormalities in predialysis, hemodialysis and peritoneal dialysis patients are analyzed. In addition, the results of the studies that tested the effects of the hypolipidemic drugs on cardiovascular morbidity and mortality in patients with CKD are reported.

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“…The large concentration gradient of Lp(a) between the aorta and renal vein [39] as well as the identification of apo(a) fragments in urine [40] suggest that the kidney may actively participate in the degradation of Lp(a). Thus, it is not surprising that patients with primary kidney diseases (even those with normal GFR values) usually exhibit markedly elevated concentrations of Lp(a) [41, 42] as well as increased concentrations of LDL-unbound apo(a) [43]. However, recently published studies indicate that the negative association between renal function and Lp(a) levels is phenotype-specific.…”

Section: Lipids In Ckd Stages 1–4mentioning

confidence: 99%